An Antitumor Immune Response Is Evoked by Partial-Volume Single-Dose Radiation in 2 Murine Models.
Animals
Antineoplastic Agents
/ therapeutic use
CD8-Positive T-Lymphocytes
/ cytology
Carcinoma, Lewis Lung
Cell Line, Tumor
DNA Damage
Disease Models, Animal
Immune System
/ radiation effects
Intercellular Adhesion Molecule-1
/ chemistry
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Nude
Microscopy, Fluorescence
Neoplasm Transplantation
Neoplasms
/ radiotherapy
Radiotherapy
/ methods
Radiotherapy Dosage
T-Lymphocytes
/ radiation effects
Journal
International journal of radiation oncology, biology, physics
ISSN: 1879-355X
Titre abrégé: Int J Radiat Oncol Biol Phys
Pays: United States
ID NLM: 7603616
Informations de publication
Date de publication:
01 03 2019
01 03 2019
Historique:
received:
14
05
2018
revised:
02
10
2018
accepted:
08
10
2018
pubmed:
21
10
2018
medline:
4
9
2019
entrez:
21
10
2018
Statut:
ppublish
Résumé
This study examined tumor growth delay resulting from partial irradiation in preclinical mouse models. We investigated 67NR murine orthotopic breast tumors in both immunocompetent and nude mice. Treatment was delivered to 50% or 100% of the tumor using a 2 × 2 cm collimator on a microirradiator. Radiation response was modulated by treatment with anti-CD8 and anti-intercellular adhesion molecule (anti-ICAM) antibodies. Similar experiments were performed using the less immunogenic Lewis lung carcinoma mouse model. Tumor growth delay and γ-H2AX phosphorylation were measured, and immune response was assessed by immunofluorescence and flow cytometry at 1 and 7 days after radiation therapy. Tumor expression of cellular adhesion molecules was also measured at different times after radiation therapy. Partial irradiation led to tumor responses similar to those of fully exposed tumors in immunocompetent mice, but not in nude mice. After a single dose of 10 Gy, infiltration of CD8 In these models, radiation controls tumor growth both directly through cell killing and indirectly through immune activation. This outcome raises the possibility that this effect could be induced in the clinic.
Identifiants
pubmed: 30342090
pii: S0360-3016(18)33860-4
doi: 10.1016/j.ijrobp.2018.10.009
pmc: PMC6764416
mid: NIHMS1533820
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
Icam1 protein, mouse
0
Intercellular Adhesion Molecule-1
126547-89-5
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
697-708Subventions
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA105125
Pays : United States
Informations de copyright
Copyright © 2018 Elsevier Inc. All rights reserved.
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